Evaluate three important aspects of the function in the ischemic kidney: (1) the pathophysiology of the kidney injured by brief or partial ischemia; (2) the function of juxtamedullary nephrons; (3) reabsorption of metabolites in tubules whose brush border has been eliminated by prior brief ischemia. Pursue our morphological studies of the ischemic kidney. (1) Describe in detail the biology of ischemic injury to brush border, using histochemical and ultrastructural techniques. (2) Analyze recovery from severe renal ischemia, using morphological and functional methods. (3) Determine whether a nephrotoxin induces the same pattern of selective cell injury we have described for brief ischemia. Determine the biochemical effects of ischemia on tubular cell membranes. Specifically, we shall: (1) determine the rate of regeneration of protein and phospholipid components of microvilli following ischemic damage; (2) test the function of transport systems during recovery by measuring the uptake of amino acids and glucose into membrane vesicles; (3) determine how binding sites on the brush border are affected by ischemic injury. Study the mechanism of action in the renal microcirculation by which mannitol alters renal hemodynamics: (a) under control conditions; (b) after total occlusion; (c) after partial arterial constriction; (d) during partial arterial constriction. Evaluate anatomical changes in the microvasculature induced by ischemia and by mannitol. Evaluate the functional significance of collateral circulation in the dog kidney during complete and partial renal artery occlusion. Define the intrarenal distribution of blood flow in both anesthetized and unanesthetized dogs during hemorrhagic hypotension and renal arterial clamping. Explore the possible roles of the sympathetic nervous system, angiotensin and prostaglandins in "patchy" cortical ischemia and in any differences between hemorrhage and clamping.